Citation: Stefanova KI, Delcheva GT, Maneva AI, Batalov AZ, Geneva-Popova MG, Karalilova RV, Simitchiev KK. Pathobiochemical mechanisms relating iron homeostasis with parameters of infl ammatory activity and autoimmune disorders in rheumatoid arthritis. Folia Med (Plovdiv) 2018;60(1):124-32.
Compliance of patients with antiresorptive therapy depends on the specific socio-economic conditions and the attending physician's behaviour. Very rarely, treatment is discontinued because of adverse effects exerted by the drugs or because patients may not be convinced that they have osteoporosis.
Introduction: TNF-α blocker therapy is part of the treatment with biologics used in the management of inflammatory joint diseases. In recent years, drug-induced neutralizing antibodies have been shown to have a negative effect on the course of the disease process. Aim: To investigate drug-induced neutralizing antibodies against TNF-α blocking drugs used in patients with inflammatory joint diseases and their effect on the clinical course of the disease. Materials and methods: The study included 121 (56.8%) patients with rheumatoid arthritis, 50 (23.5%) patients with ankylosing spondylitis, 42 (19.7%) patients with psoriatic arthritis, and 31 sex and age-matched healthy controls. The patients were monitored at 0, 6, 12, and 24 months after initiation of TNF-α blocker treatment. The demographic data, vital signs and the parameters of inflammatory activity (C-reactive protein, erythrocyte sedimentation rate, and disease activity indices) were analyzed in all patients. Drug-induced anti-TNF-α blockers antibodies (adalimumab and etanercept) were analyzed using ELISA. Statistical analysis was performed with SPSS v. 24. Results: Drug-induced neutralizing antibodies against adalimumab were obtained in 11.57% of patients at 6 month, in 17.64% at 12 month, and in 24.8% at 24 month. Drug-induced neutralizing antibodies to etanercept were not demonstrated in patients followed up at 6 months, at 7.77% at 12 months, and at 9.63% at 24 months. Between the presence of neutralizing antibodies to blockers of TNF-α and indices available for disease activity, there is a strong positive correlation and Pearson Correlation = 0.701, p=0.001. Patients with poor clinical response and available antibodies against adalimumab at 12 months were 82.36% and patients treated with etanercept 71.42%. The difference between the two groups was non-significant (U = 0.527, p> 0.05). Patients with poor clinical response and available anti-adalimumab antibodies at 24 month were 75%, and in patients treated with etanercept – 87.50%, the difference between the two groups not being able to reach significance (U = 0.623, p> 0.05). Conclusion: Drug-induced neutralizing antibodies against TNF-α blockers (adalimumab and etanercept) have a negative effect on the course of inflammatory joint disease and can be used as reliable biomarker to assess the effect of the treatment with these drugs.
Introduction: Data on the associations between capillaroscopic changes and diagnostic systemic-sclerosis (SSc)-related antibodies are scarce. Presence of such correlation would improve current knowledge about the disease’s pathogenesis by revealing the mechanisms of microangiopathy. The microvascular pathology of SSc is a hallmark of the disease, and immunological abnormalities probably contribute to its development. Patients and methods: 19 patients with definite diagnosis of SSc were included in the current pilot study; 16 had limited and 3 had diffuse cutaneous involvement; their mean age was 51.56 ± 15.07 years. All patients exhibited symptoms of Raynaud’s phenomenon of the fingers. A “scleroderma” type capillaroscopic pattern was classified according to the staging suggested by Cutolo et al. (2000): “early”, “active” or ”late” phase. In the presence of different degrees of capillaroscopic changes in different fingers, the most-advanced microvascular pathology was chosen for classification. In cases without capillaroscopic features of microangiopathy, the findings were categorized as normal or nonspecific (dilated, tortuous capillaries, and/or hemorrhages). Indirect immunofluorescence on HEp-2 cells was performed as the gold-standard screening method for the detection of antinuclear autoantibodies (ANA), and determination of the immunofluorescent staining pattern (anti-cell pattern) was in accordance with the International Consensus on ANA Patterns. Scleroderma-associated autoantibodies in the patients’ serum were assessed using line immunoblot assay for detection of autoantibodies to 13 scleroderma-associated autoantigens: Scl-70, CENP A, CENP B, RP11/RNAP-III, RP155/RNAP-III, fibrillarin, NOR-90, Th/To, PM-Scl100, PM-Scl75, Ku, PDGFR, and Ro-52. Results: In 73.7% (n = 14) of the examined patients, “scleroderma” type capillaroscopic changes were found, and in 26.3% (n = 5), capillaroscopic features of microangiopathy were absent (nonspecific changes, n = 3; normal findings, n = 2). In SSc patients with positive anti-Scl-70 (n = 7) antibodies, significantly lower mean capillary density was observed along with a higher frequency of “active” and “late” phase capillaroscopic changes as compared to the anti-Scl-70-negative patients (p < 0.05). Anti-RNAP III–155 positive patients (n = 4) had significantly higher mean capillary density than anti-RNAP III–155 negative patients (n = 15). In three of the anti-RNAP III–155-positive cases, capillaroscopic features of microangiopathy were not detected, and in one case there was an “early” phase “scleroderma” pattern. Conclusion: In the current pilot study, the association between more advanced capillaroscopic changes and the presence of anti-Scl-70 autoantibodies was confirmed. As a novel observation, positive anti-RNAP III–155 antibodies were found in SSc patients with or without early microangiopathy. The question of associations between microvascular changes in SSc and other SSc-related autoantibodies requires further research.
The role of IFN-α-induced chemokines CCL2, CXCL10 and CCL19 in different forms of SLE has not been studied in Bulgaria, with worldwide sources attributing varying degrees of importance. The aim of this study was to investigate the correlation between IFN-induced chemokines CCL2, CXCL10 and CCL19 and disease activity in patients with SLE over 24 months. Materials and methods: This study used data from 70 patients with SLE (age range 24–62 years) and a control group of 30 healthy volunteers matched for age and gender. Levels of chemokines CCL2, CXCL10 and CCL19 in lupus patients’ serum were measured by ELISA. The study examined clinical and clinical laboratory indicators, as well as measures of disease activity developed for lupus patients (SLEDAI and SLICC). Statistical program SPSS, Version 26 were used for statistical data processing with p < 0.05. At 24 months of follow-up, 12 patients were with deterioration, and they had an IFN-a of 363.76 ± 9.23 versus 116.1 ± 22.1 pg/mL of those who did not worsen, CCL2 278.3 ± 5.12 versus 89.4 ± 12.8, CXCL10 234.2 ± 6.13 versus 115.23 ± 5.9 p CCL19 776.25 ± 5.1 vs. 651.34 ± 9.0 during the first visit. Results: The mean values of CCL2, CXCL10 and CCL19 were higher in patients with SLE compared to healthy controls (p = 0.01). A strong significant association (p = 0.01) was found between the concentration of CCL2, CXCL10 and CCL19 and with patients’ age, disease duration, SLEDAI and SLICC. Conclusion: CCL2, CXCL10 and CCL19 serum levels were found to correlate with patients’ age and disease duration. The level of IFN-induced chemokines CCL2, CXCL10 and CCL19 has a prognostic value in terms of SLE disease activity and degree of organ damage.
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